Evidence map›Paper›PMID 22461891›Full record

ArticlePloS one2012

CIP2A promotes proliferation of spermatogonial progenitor cells and spermatogenesis in mice.

Sami Ventelä, Christophe Côme, Juho-Antti Mäkelä, Robin M Hobbs, Leni Mannermaa, Markku Kallajoki, Edward K Chan, Pier Paolo Pandolfi, Jorma Toppari, Jukka Westermarck

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
6.9field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Leucine-rich repeat-containing protein 59 mediates nuclear import of cancerous inhibitor of PP2A in prostate cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 5 institutions in 2 countries.

Sami VenteläTurku Centre for Biotechnology, University of Turku, Turku, Finland.
Christophe Côme
Juho-Antti Mäkelä
Robin M Hobbs
Leni Mannermaa
Markku Kallajoki
Edward K Chan
Pier Paolo Pandolfi
Jorma Toppari
Jukka Westermarck
University of Turku · FIÅbo Akademi University · FIBeth Israel Deaconess Medical Center · USCancer Genetics (United States) · USUniversity of Florida · US

Funding

UF Clinical and Translational Science AwardUL1TR000064 · NCATS · UNIVERSITY OF FLORIDA · PI NELSON, DAVID R · 2012 to 2014
$12.2M
NCATS NIH HHS UL1 TR000064Worldwide Cancer Research 08-0614
6 · The paper itself

Abstract

Protein phosphatase 2A (PP2A) is a critical regulator of protein serine/threonine phosphorylation. However, the physiological and developmental roles of different PP2A complexes are very poorly understood. Here, we show that a newly characterized PP2A inhibitory protein CIP2A is co-expressed with ki-67 and with self-renewal protein PLZF in the spermatogonial progenitor cell (SPC) population in the testis. CIP2A and PLZF expression was shown also to correlate Ki-67 expression in human testicular spermatogonia. Functionally, CIP2A mutant mouse testes exhibited smaller number of PLZF-positive SPCs and reduced sperm counts. Moreover, seminiferous tubuli cells isolated from CIP2A mutant mice showed reduced expression of Plzf and other renewal genes Oct-4 and Nanog at mRNA level. However, PLZF-deficient testes did not show altered CIP2A expression. Importantly, spermatogonia-specific restoration of CIP2A expression rescued PLZF expression and sperm production defects observed in CIP2A mutant mice. Taken together, these results reveal first physiological function for an emerging human oncoprotein CIP2A, and provide insights into maintenance of PLZF-positive progenitors. Moreover, demonstration that CIP2A expression can be systematically inhibited without severe consequences to normal mouse development and viability may have clinical relevance regarding targeting of oncogenic CIP2A for future cancer therapies.

Indexed as

Cell ProliferationAnimalsAutoantigensFemaleGene Expression Regulation, DevelopmentalHumansImmunohistochemistryKruppel-Like Transcription FactorsMaleMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutPromyelocytic Leukemia Zinc Finger ProteinReverse Transcriptase Polymerase Chain ReactionRNA InterferenceAutoantigensKIAA1524 protein, mouseKruppel-Like Transcription FactorsMembrane ProteinsPromyelocytic Leukemia Zinc Finger ProteinZbtb16 protein, mouse

Identifiers

PMID22461891
PMCPMC3312892
OpenAlexW2073664416

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.